Evidence map›Paper›PMID 38464047›Full record

ArticlebioRxiv : the preprint server for biology2024

Preclinical assessment of MAGMAS inhibitor as a potential therapy for pediatric medulloblastoma.

Zahra Motahari, Javier J Lepe, Malia R Bautista, Clay Hoerig, Ashley S Plant-Fox, Bhaskar Das, Christie D Fowler, Suresh N Magge, Daniela A Bota

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Zahra MotahariCHOC Neuroscience Institute, Children's Hospital of Orange County, Orange, CA, USA.
Javier J LepeDepartment of Neurology, School of Medicine, University of Irvine, CA, USA.ORCID 0000-0001-8956-6999
Malia R BautistaDepartment of Neurobiology and Behavior, School of Biological Sciences, University of California, Irvine, CA, USA.
Clay HoerigDepartment of Pediatric Oncology, Children's Hospital of Orange County, Orange, CA, USA.
Ashley S Plant-FoxDepartment of Pediatric Oncology, Children's Hospital of Orange County, Orange, CA, USA.
Bhaskar DasArnold and Marie Schwartz College of Pharmacy and Health Sciences, Long Island University, Brooklyn, NY, USA.
Christie D FowlerDepartment of Neurobiology and Behavior, School of Biological Sciences, University of California, Irvine, CA, USA.ORCID 0000-0003-2864-2163
Suresh N MaggeCHOC Neuroscience Institute, Children's Hospital of Orange County, Orange, CA, USA.
Daniela A BotaDepartment of Neurology, School of Medicine, University of Irvine, CA, USA.ORCID 0000-0002-9680-9060
University of California, Irvine · USChildren's Hospital of Orange County · USLong Island University · USLurie Children's Hospital · USUniversity of Minnesota · US

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Christine Hui · 1994 to 2026
$57.9M
Targeting of Mitochondrial Lon Protease as a Novel Therapy for GlioblastomaR01NS109423 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BOTA, DANIELA ANNENELIE, DAS, BHASKAR CHANDRA · 2020 to 2024
$2.3M
NCI NIH HHS P30 CA062203NINDS NIH HHS R01 NS109423
6 · The paper itself

Abstract

Medulloblastoma, the most common pediatric brain malignancy, has Sonic Hedgehog (SHH) and non-SHH group3 subtypes. MAGMAS (Mitochondrial Associated Granulocyte Macrophage colony-stimulating factor Signaling molecules) encode for mitochondrial import inner membrane translocase subunit and is responsible for translocation of matrix proteins across the inner membrane. We previously reported that a small molecule MAGMAS inhibitor, BT9, decreases cell proliferation, migration, and oxidative phosphorylation in adult glioblastoma cell lines. The aim of our study was to investigate whether the chemotherapeutic effect of BT9 can be extended to pediatric medulloblastoma. Methods: Multiple in vitro assays were performed using human DAOY (SHH activated tp53 mutant) and D425 (non-SHH group 3) cells. The impact of BT9 on cellular growth, death, migration, invasion, and metabolic activity were quantified using MTT assay, TUNEL staining, scratch wound assay, Matrigel invasion chambers, and seahorse assay, respectively. Survival following 50mg/kg BT9 treatment was assessed Results: Compared to control, BT9 treatment led to a significant reduction in medulloblastoma cell growth (DAOY, 24hrs IC50: 3.6uM, 48hrs IC50: 2.3uM, 72hrs IC50: 2.1uM; D425 24hrs IC50: 3.4uM, 48hrs IC50: 2.2uM, 72hrs IC50: 2.1uM) and a significant increase in cell death (DAOY, 24hrs p=0.0004, 48hrs p<0.0001; D425, 24hrs p=0.0001, 48hrs p=0.02). In DAOY cells, 3uM BT9 delayed migration, and significantly decreased DAOY and D425 cells invasion (p < 0.0001). Our Conclusions: Our

Identifiers

PMID38464047
PMCPMC10925277
OpenAlexW4392362618

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.